Sentence examples for blockade of cell binding from inspiring English sources

Exact(1)

A blockade of cell binding by immune serum neutralizes murine gamma-herpesvirus-68 (MHV-68) for infection of FcR− cells, but not FcR+ cells [17].

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Although these data indicate that Ag-PS-10 and AgNO3 decrease MPV plaque formation, the mechanism by which this inhibition occurs is not known and could involve blockade of host cell binding, disruption of host cell biochemical pathways, or both.

Experimentally this has been achieved by neutralisation of transforming growth factor-beta over the first 3 days following injury, or by blockade of inflammatory cell binding to the CS-1 locus on fibronectin with an anti-VLA-4 antibody, or with the synthetic VLA-4 inhibitor, CS-1 peptide, in a rat model of tendon transection.

It is unclear why we did not observe a complete correlation between binding to ubiquitinated RIP1 and blockade of cell death.

Using cell adhesion assay, we found that blockade of cell surface GRP78 with the NTD antibody decreased the binding ability of tumor cells to fibronectin in QGY-7703 cells (Fig.  1h).

In NCCIT cells, blockade of Cripto binding to cell surface GRP78 using the antibody against the NH2-terminal domain inhibited tumor cell proliferation, suggesting that the NH2-terminal domain of cell surface GRP78 also plays a pro-proliferative role in NCCIT cells [ 26].

This effect was presumably due to blockade of HMGB1 binding to cell surface receptors, thereby attenuating its pro-inflammatory capability [ 11].

BAFF-R was expressed on the cell membrane of human mesangial cells and blockade of BAFF/BAFF-R binding abrogated the proliferative effect of BAFF on human mesangial cells.

Selective blockade of VEGF binding to VEGFR2 by r84 is shown through ELISA, receptor binding assays, receptor activation assays, and cell-based functional assays.

Coregulator recruitment is a crucial regulatory step in AR signaling and the direct blockade of coactivator binding to AR offers the opportunity to develop therapeutic agents that would remain effective in prostate cancer cells resistant to conventional endocrine therapies.

Importantly, blockade of PI3K binding to PDGFRβ did not suppress over-activation of TGFβ signaling (Figure 6A).

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